Acute pancreatitis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
The two types of pancreatitis are mild pancreatitis and severe pancreatitis, which are separated based on whether their predominant response to cell injury is inflammation or necrosis, respectively. In mild pancreatitis there is inflammation and edema of the pancreas. In severe pancreatitis there are additional features of necrosis and secondary injury to extrapancreatic organs. Both types share a common mechanism of abnormal inhibition of secretion of [[zymogens]] and inappropriate activation of pancreatic zymogens inside the pancreas, most notably [[trypsinogen]]. Normally, trypsinogen is activated to [[trypsin]] in the duodenum where it assists in the digestion of proteins. During an acute pancreatitis episode there is colocalization of lysosomal enzymes, specifically [[cathepsin]], with trypsinogen. Cathepsin activates trypsinogen to trypsin leading to further activation of other molecules of trypsinogen and immediate pancreatic cell death according to either the necrosis or apoptosis mechanism (or a mix between the two). The balance between these two processes is mediated by [[caspases]] which regulate apoptosis and have important anti-necrosis functions during pancreatitis: preventing trypsinogen activation, preventing ATP depletion through inhibiting polyADP-ribose polymerase, and by inhibiting the inhibitors of apoptosis (IAPs). If, however, the caspases are depleted due to either chronic ethanol exposure or through a severe insult then necrosis can predominate. | The two types of [[pancreatitis]] are mild pancreatitis and severe pancreatitis, which are separated based on whether their predominant response to cell injury is inflammation or necrosis, respectively. In mild pancreatitis there is [[inflammation]] and [[edema]] of the pancreas. In severe pancreatitis there are additional features of necrosis and secondary injury to extrapancreatic organs. Both types share a common mechanism of abnormal inhibition of secretion of [[zymogens]] and inappropriate activation of pancreatic zymogens inside the pancreas, most notably [[trypsinogen]]. Normally, [[trypsinogen]] is activated to [[trypsin]] in the duodenum where it assists in the digestion of proteins. During an [[acute pancreatitis]] episode there is colocalization of [[lysosomal enzymes]], specifically [[cathepsin]], with trypsinogen. [[Cathepsin]] activates trypsinogen to trypsin leading to further activation of other molecules of trypsinogen and immediate pancreatic cell death according to either the [[necrosis]] or [[apoptosis]] mechanism (or a mix between the two). The balance between these two processes is mediated by [[caspases]] which regulate apoptosis and have important anti-necrosis functions during pancreatitis: preventing trypsinogen activation, preventing ATP depletion through inhibiting polyADP-ribose polymerase, and by inhibiting the inhibitors of apoptosis (IAPs). If, however, the caspases are depleted due to either chronic ethanol exposure or through a severe insult then necrosis can predominate. | ||
===Microscopic Pathology=== | ===Microscopic Pathology=== | ||
The acute pancreatitis (acute hemorrhagic pancreatic necrosis) is characterized by acute inflammation and necrosis of pancreas parenchyma, focal enzymic necrosis of pancreatic fat and vessels necrosis - hemorrhage. These are produced by intrapancreatic activation of pancreatic enzymes. Lipase activation produces the necrosis of fat tissue in pancreatic interstitium and peripancreatic spaces. Necrotic fat cells appear as shadows, contours of cells, lacking the nucleus, pink, finely granular cytoplasm. It is possible to find calcium precipitates (hematoxylinophilic). Digestion of vascular walls results in thrombosis and hemorrhage. Inflammatory infiltrate is rich in [[neutrophils]]. Photos at: [http://www.pathologyatlas.ro/Acute%20Pancreatitis.html Atlas of Pathology] | The acute pancreatitis (acute hemorrhagic pancreatic necrosis) is characterized by acute inflammation and necrosis of pancreas parenchyma, focal enzymic necrosis of pancreatic fat and vessels necrosis - hemorrhage. These are produced by intrapancreatic activation of [[pancreatic enzymes]]. [[Lipase]] activation produces the necrosis of fat tissue in pancreatic interstitium and peripancreatic spaces. Necrotic fat cells appear as shadows, contours of cells, lacking the nucleus, pink, finely granular cytoplasm. It is possible to find calcium precipitates (hematoxylinophilic). Digestion of vascular walls results in thrombosis and hemorrhage. Inflammatory infiltrate is rich in [[neutrophils]]. Photos at: [http://www.pathologyatlas.ro/Acute%20Pancreatitis.html Atlas of Pathology] | ||
==References== | ==References== | ||
Revision as of 20:47, 16 August 2012
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Acute pancreatitis Microchapters |
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Acute pancreatitis pathophysiology On the Web |
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American Roentgen Ray Society Images of Acute pancreatitis pathophysiology |
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Risk calculators and risk factors for Acute pancreatitis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2]
Overview
Pathophysiology
The two types of pancreatitis are mild pancreatitis and severe pancreatitis, which are separated based on whether their predominant response to cell injury is inflammation or necrosis, respectively. In mild pancreatitis there is inflammation and edema of the pancreas. In severe pancreatitis there are additional features of necrosis and secondary injury to extrapancreatic organs. Both types share a common mechanism of abnormal inhibition of secretion of zymogens and inappropriate activation of pancreatic zymogens inside the pancreas, most notably trypsinogen. Normally, trypsinogen is activated to trypsin in the duodenum where it assists in the digestion of proteins. During an acute pancreatitis episode there is colocalization of lysosomal enzymes, specifically cathepsin, with trypsinogen. Cathepsin activates trypsinogen to trypsin leading to further activation of other molecules of trypsinogen and immediate pancreatic cell death according to either the necrosis or apoptosis mechanism (or a mix between the two). The balance between these two processes is mediated by caspases which regulate apoptosis and have important anti-necrosis functions during pancreatitis: preventing trypsinogen activation, preventing ATP depletion through inhibiting polyADP-ribose polymerase, and by inhibiting the inhibitors of apoptosis (IAPs). If, however, the caspases are depleted due to either chronic ethanol exposure or through a severe insult then necrosis can predominate.
Microscopic Pathology
The acute pancreatitis (acute hemorrhagic pancreatic necrosis) is characterized by acute inflammation and necrosis of pancreas parenchyma, focal enzymic necrosis of pancreatic fat and vessels necrosis - hemorrhage. These are produced by intrapancreatic activation of pancreatic enzymes. Lipase activation produces the necrosis of fat tissue in pancreatic interstitium and peripancreatic spaces. Necrotic fat cells appear as shadows, contours of cells, lacking the nucleus, pink, finely granular cytoplasm. It is possible to find calcium precipitates (hematoxylinophilic). Digestion of vascular walls results in thrombosis and hemorrhage. Inflammatory infiltrate is rich in neutrophils. Photos at: Atlas of Pathology